bubble_chart Overview

Forest encephalitis, also known as tick-borne encephalitis, is an acute infectious disease caused by a virus. It was first discovered in the forested areas of eastern Russia from May to August 1934, hence it is also called Russian spring-summer encephalitis. Wild animals, particularly wild rodents, are the source of infection, with ticks serving as the transmission vector. Clinically, it is characterized by sudden high fever, meningeal irritation, impaired consciousness, and paralysis. Abnormal changes in cerebrospinal fluid are observed, and sequelae are common.

bubble_chart Epidemiology

The epidemic of this disease exhibits a strict seasonality, beginning in early May, peaking in June, and declining from July to August, presenting a sporadic pattern. Approximately 80% of cases occur between May and June. The distribution of this disease is strictly regional, primarily observed in the virgin forest areas of northeastern and northwestern China. The population is generally susceptible, with all patients associated with forest-related activities, particularly among lumberjacks, and predominantly affecting young adults aged 20–30. A relatively long-lasting immunity can be acquired after infection.

In nature, the virus circulates between ticks and wild animals, with rodents such as squirrels, field mice, and hedgehogs serving as pestilence sources. When ticks feed on the blood of infected rodents, the virus multiplies within the ticks and can overwinter or be transmitted transovarially. Thus, ticks are not only vectors but also important reservoir hosts. When susceptible individuals enter forested areas where the disease is endemic and are bitten by virus-carrying ticks, they may become infected. Most cases result in asymptomatic or mild infections, with only a small proportion developing typical symptoms.

bubble_chart Pathogen

The pathogen of this disease belongs to the Flavivirus genus of the membrane virus, specifically the fourth subgroup. It exhibits icosahedral symmetry with a diameter of 30 nm, enveloped by a reticular lipoprotein membrane, giving it a spherical appearance. Inside, there is a core surrounded by a protein capsid, containing single-stranded RNA. The pathogen can be isolated from the brain tissue of patients within 7 days of onset and can also be detected in other organs and body fluids, such as the spleen, liver, blood, cerebrospinal fluid, and urine, albeit with a lower positive rate. The most commonly used laboratory animals are white mice and suckling mice, inoculated intracerebrally, and the virus can also grow in chicken embryos or cell cultures. The virus has low resistance to external factors, being immediately killed by boiling and inactivated after heating at 60°C for 10 minutes. It is sensitive to ether and acetone. The virus can be preserved in brain tissue for 70 days, in 50% glycerol for over 3 months (at 4°C), and for even longer under low warm purgation.

Approximately 10% of patients develop neutralizing antibodies in their serum 15 days after the onset, which can persist for a long time. Complement-fixing antibodies begin to appear one month after infection and significantly decline after six months. Hemagglutination-inhibiting antibodies appear earlier and remain in the serum for a longer duration.

bubble_chart Pathogenesis

After the virus invades the human body, it replicates in the mononuclear-phagocyte system, such as local lymph nodes, before entering the bloodstream and causing viremia. Due to the formation of specific antibodies, most patients experience latent infections or present as mild atypical cases. Only a small proportion of patients develop lesions when the virus enters the central nervous system. In experimental infections in mice, the virus is present in the lymphatic system and bloodstream within the first 48 hours, then spreads to the brain and other organs. The viral load in the brain peaks after 8 days, while in other organs, it gradually declines due to the emergence of specific antibodies.

bubble_chart Pathological Changes

The pathological changes of this disease are similar to those of Japanese encephalitis, with widespread inflammatory lesions in the nervous system involving the gray matter, white matter, and meninges. There are exudative and degenerative changes, along with glial cell reactions and perivascular cuffing of lymphocytes. Neuronal degeneration, necrosis, and softening foci in the brain tissue are common, often affecting the basal ganglia, thalamus, and brainstem. The spinal cord may also be involved, particularly the upper cervical segments. In severe cases, the lesions may extend to the medulla oblongata. Apart from the nervous system, degenerative changes may also occur in the heart, liver, and kidneys.

bubble_chart Clinical Manifestations

The incubation period is generally 10 to 15 days, but can be as long as 1 month. Patients with the ordinary type experience an acute onset, reaching peak severity within 1 to 2 days, and exhibit varying degrees of consciousness impairment, neck and limb paralysis, and meningeal irritation. Mild cases often have a gradual onset, with prodromal symptoms such as fever, headache, generalized soreness, tinnitus, and loss of appetite, followed by neurological symptoms after 3 to 4 days. Severe cases have a sudden onset, with abrupt high fever or hyperpyrexia, accompanied by headache, nausea, vomiting, hyperesthesia, and consciousness impairment, rapidly progressing to meningeal irritation and culminating in unconsciousness, spasms, and bulbar paralysis within hours, leading to death.

Fever is typically above 38°C, lasting 5 to 10 days in most cases, with sustained fever being the most common pattern, though biphasic or remittent fever may also occur. Occasionally, hemorrhagic rashes appear, and some cases exhibit myocarditis symptoms.

Neurological symptoms primarily include consciousness impairment, meningeal irritation signs, and paralysis. Over half of the cases exhibit varying degrees of consciousness impairment, ranging from drowsiness, delirium, and stupor to deep unconsciousness. Some may present with agitation, convulsions, and mental confusion. Consciousness impairment gradually improves as body temperature subsides.

Meningeal irritation signs are the earliest and most common symptoms and signs, beginning with severe headache of variable location, followed by nausea and vomiting. These signs typically persist for 5 to 10 days and may remain even after consciousness is restored.

Paralysis mainly affects the neck, scapular muscles, and upper limbs, followed by hemiplegia and lower limb paralysis. Cranial nerve paralysis is rare. Unlike Japanese encephalitis, the paralysis in this disease is flaccid and often occurs between the 2nd and 5th days of illness. When the neck or scapular muscles are involved, the characteristic symptom of head drooping appears. Paralysis generally recovers gradually over 2 to 3 weeks, with muscle atrophy occurring in about half of the cases. Pathological reflexes are common, and some cases exhibit extrapyramidal signs such as tremors and involuntary movements. Occasionally, bulbar involvement symptoms like speech impairment and dysphagia may occur.

The duration of the disease varies, typically around 1 week. Symptoms gradually subside after body temperature normalizes, but paralysis may persist.

bubble_chart Auxiliary Examination

Collect paired serum samples from patients for hemagglutination inhibition test, neutralization test, complement fixation test, and enzyme-linked immunosorbent assay (ELISA). A fourfold or greater rise in antibody titer is considered diagnostically significant. For fatal cases, brain tissue can be used to isolate the virus by intracerebral inoculation in mice or by culturing with Vero cells or BHK-21 cells.

bubble_chart Diagnosis

The diagnosis is primarily based on epidemiological data such as the season of onset, occupation, and region of occurrence, combined with clinical manifestations like sudden high fever, impaired consciousness, meningeal irritation signs, and muscle paralysis. Laboratory tests are required for confirmation.

bubble_chart Treatment Measures

Early diagnosis and treatment of patients in the initial stage [first stage] can involve administering serum from convalescent patients, with daily intramuscular injections of 20–40 ml until body temperature drops below 38.5°C. Management of symptoms such as high fever, unconsciousness, convulsions, and respiratory failure follows the same approach as for Japanese encephalitis. Rehabilitation measures such as acupuncture, tuina, physiotherapy, and physical therapy can be used for sequelae like paralysis.

bubble_chart Prevention

This disease has a strict regional distribution. Forestry workers entering endemic areas must take the following measures.

1. Vaccination with tick-borne encephalitis tissue culture vaccine: the first intramuscular injection of 2.0ml, followed by another 3.0ml intramuscular injection after 7-10 days, can achieve good immunization effects.

2. Maintain good environmental hygiene around the workplace, and strengthen rodent control, extermination, and tick elimination efforts.

3. When working in forested areas, take personal protective measures by wearing tight-fitting protective clothing with secured cuffs, collars, and pant legs to prevent tick bites.